丹参素对大鼠心肌缺血/再灌注损伤的保护作用

The protection of DS-182 during reperfusion of total ischernia heart

本实验采用Langendorff灌注模型,对心肌缺血/再灌注损伤中氧自由基清除酶系统超氧化物歧化酶(SOD)、谷胱甘肽过氧化酶(GSH-P_x)和超微结构的变化及丹参素的抗氧化效应进行了观察。随缺血时间的延长,SOD及GSH-P_x的活性逐步下降。当心肌缺血40分钟后富氧再灌注20分钟,SOD的活性仍然继续下降;GSH-P_x的活性明显低于缺血60分钟组,此时超微结构损伤最为严重。预先给丹参素及亚硒酸钠再进行缺血/再灌注,心肌SOD、GSH-P_x活性明显高于单纯缺血/再灌注时,超微结构损伤亦较轻,且丹参素的保护效果优于亚硒酸钠。

The role of oxygen free radical's scavenger systems in the protection of cellular damages during total ischemia and reperfusion was studied in isolated Langendorff perfused rat hearts. The changes of myocardial enzymes(superoxide dismutase and glutathione peroxidase)and ultrastructure were used as indexes of cellular damage. The hearts were perfused in total ischemia for 40, 60, 80 min and reperfusion for an additional 20 min resulted in a decrease in both SOD and GSH-Px activity. SOD activty decreased continuously when the hearts perfused in total ischemia for periods of 40 and 60min were reperfused for an additional 20min. GSH-Px activity was much lower during reperfusion(total ischemia 40 min and reperfusion 20 min) than that during total ischemia(60 min) and ultrastrcture damage in this phase was the most severe. Both sodium selenite(Na_2SeO_3 3×10^(-8)M)and DS-182(4×10^(-6)g/ml, one of the effective components of salvia miltiorrhiza bunge) could increase the activity in both SOD and GSH-Px and protect the ultrastreture of myocardium from reperfusion injury. The DS-182 is more effective than Na_2SeO_3 in the protection of myocardium from reperfusion damage.